Key result
Intravenous atropine blunts exercise-induced muscle Oxy-Hb increases and abolishes responses during motor imagery.
Why the study?
Does intravenous atropine reduce centrally-induced cholinergic vasodilatation in skeletal muscles during one-legged exercise and motor imagery in healthy men?
Does intravenous atropine reduce centrally-induced cholinergic vasodilatation in skeletal muscles during one-legged exercise and motor imagery in healthy men?
p-value: p=<0.05
Central command evokes sympathetic cholinergic vasodilatation equally in bilateral skeletal muscles during early voluntary exercise and motor imagery.
Supports central command cholinergic vasodilatation in skeletal muscle; hypothesis-generating and does not alter clinical practice.
We have recently reported that central command contributes to increased blood flow in both noncontracting and contracting vastus lateralis (VL) muscles at the early period of voluntary one-legged cycling. The purpose of this study was to examine whether sympathetic cholinergic vasodilatation mediates the increases in blood flows of both muscles during one-legged exercise. Following intravenous administration of atropine (10 μg/kg), eight subjects performed voluntary 1-min one-legged cycling (at 35% of maximal voluntary effort) and mental imagery of the exercise. The relative concentrations of oxygenated- and deoxygenated-hemoglobin (Oxy- and Deoxy-Hb) in the bilateral VL were measured as an index of muscle tissue blood flow with near-infrared spectroscopy (NIRS). The Oxy-Hb in both noncontracting and contracting VL increased at the early period of one-legged cycling, whereas the Deoxy-Hb did not alter at that period. Atropine blunted (P < 0.05) the Oxy-Hb responses of both VL muscles but did not affect the Deoxy-Hb responses. The time course and magnitude of the atropine-sensitive component in the Oxy-Hb response were quite similar between the noncontracting and contracting VL muscles. With no changes in the Deoxy-Hb and hemodynamics, imagery of one-legged cycling induced the bilateral increases in the Oxy-Hb, which were completely abolished by atropine. In contrast, imagery of a circle (with no relation to exercise) did not alter the NIRS signals, irrespective of the presence or absence of atropine. It is concluded that central command evokes cholinergic vasodilatation equally in bilateral VL muscles during voluntary one-legged cycling and motor imagery.
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Ishii et al. (2013) studied Healthy individuals (n=8). Atropine vs. Control (no atropine) was evaluated on Relative concentration of oxygenated-hemoglobin (Oxy-Hb) in the bilateral vastus lateralis muscles (p=<0.05). Intravenous atropine significantly blunted the initial peak changes of Oxy-Hb in bilateral vastus lateralis muscles during voluntary one-legged cycling and completely abolished the centrally induced increases during motor imagery.
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